The concept of "sodium-dependent" hypertension is based almost entirely on studies in which the dietary intake of sodium (Na+) has been varied by varying the intake of sodium chloride (NaC1). The dietary intake of chloride might also be a determinant of blood pressure (BP). If so, "hidden" sources of dietary Na+ such as sodium bicarbonate (NaHCO3) or sodium ascorbate may be as important in the pathogenesis of hypertension as has been widely believed. In chronic metabolic balance studies in patients with "salt-sensitive" essential hypertension, in spontaneously hypertensive rats, and in rats with a reduction in functional renal mass, we will determine whether changes in dietary NaC1 induce changes in blood pressure different from those induced by changes in dietary sodium citrate, bicarbonate, or ascorbate. The changes in body weight, extracellular fluid volume, and external balances of sodium, potassium, chloride, calcium, magnesium, and phosphorus induced by changing the intake of the different sodium salts will also be determined. In uninephrectomized rats given desoxycorticosterone (DOC), we will attempt to determine whether the finding that a normal amount of dietary NaC1 induces hypertension, whereas an equimolar amount of dietary NaHCO3 does not, is due to a hypertensive effect of chloride, or to an anti-hypertensive effect of bicarbonate. Accordingly, in uninephrectomized rats given DOC, we will determine; 1) whether supplemental dietary NaHCO3 can attenuate the hypercalciuric and hypertensive effects of a normal amount of dietary NaC1; 2) whether a non-halide Na+ salt that does not induce the severe alkalosis induced by NaHCO3 (e.g. sodium caseinate), still fails to induce hypertension; 3) whether a normal amount of dietary NaC1 gives rise to a serum level of parathyroid hormone (PTH) greater than that which attends an equimolar amount of dietary NaHCO3 and whether exogenously administered PTH can induce hypertension in rats given this amount of NaHCO3; 4) whether the antihypertensive effect of supplemental dietary calcium carbonate is greater than that of supplemental dietary calcium chloride; 5) whether a normal amount of dietary NaC1 gives rise to greater levels of plasma volume, cardiac output, or sympathetic nervous system activity, or lower levels of vascular smooth muscle sodium-potassium ATPase activity, than those which attend an equimolar amount of dietary NaHCO3.